After a distressing event, intrusive reexperiencing symptoms (i.e., cued memories, nightmares, out-of-the- blue intrusions) often persist and, for some, become pathological (e.g., Brewin et al., 2010). Intrusions are understudied and debilitating, and it is thus imperative that we enhance our understanding of the mechanisms behind their development, persistence, and reduction. Exposure-based therapies aimed at reducing intrusions are derived from fear conditioning and extinction models (e.g., Garakani et al., 2006); methods that enhance extinction may translate to improved treatments. One possible opportunity for enhancing extinction is through memory reconsolidation (Duvarci & Nader, 2004; Monfils et al., 2009). A retrieved memory enters a labile state as proteins are synthesized, and the effects of new learning that occurs during protein synthesis are more robust (e.g., Nader et al., 2000). In animals, retrieving a memory via a conditioned stimulus (CS) cue and then modifying the retrieved memory behaviorally through fear extinction within a specific reconsolidation window may lead to more robust effects of extinction (e.g., Monfils et al., 2009; Rao-Ruiz et al., 2011). To date, memory reconsolidation research in humans, using basic fear acquisition and extinction paradigms, have been limited to methods that do not mirror clinical complexity of stimuli seen in pathological fear learning and extinction. Further, none of this research has examined intrusive reexperiencing or neurobiological mechanisms such as noradrenergic activity and cortisol linked to behavioral modifications within the reconsolidation window. In a two-study sequence, we will examine both behavioral and biological mechanisms underlying memory reconsolidation, first in a non-clinical adult sample, and then in a sample of trauma- exposed adults with and without clinical levels of intrusive reexperiencing. We will use a fear learning and extinction distressing film paradigm in order to induce and later reduce intrusive reexperiencing. Prior to extinction, participants will be randomized to CS cueing conditions inside and outside of the reconsolidation window. Intrusive reexperiencing will be assessed 24 h and 72 h after extinction. In addition, cortisol and salivary alpha amylase (in non-clinical study) and norepinephrine (in clinical study), biomarkers associated with stress and memory, will be assessed throughout. This study will use real-world stimuli to translate animal models of memory reconsolidation to a non-clinical sample, and then will further extend to a clinical sample, examining a real clinical phenotype, intrusive reexperiencing, in both studies. Memory reconsolidation may be a mechanism to enhance fear extinction in humans, and has potentially important and exciting clinical applications for improving therapies that target intrusive re-experiencing.